The recovery of this cold-adapted bacterium from a neutral Arctic thermal spring increases our knowledge of the diversity and adaptation of extremophilic gammaproteobacterial methanotrophs in the candidate family "Methylomonadaceae".In light of the recent pandemic, favipiravir (Avigan®), a purine nucleic acid analog and antiviral agent approved for use in influenza in Japan, is being studied for the treatment of coronavirus disease 2019 (COVID-19). Increase in blood uric acid level is a frequent side effect of favipiravir. Here, we discussed the mechanism of blood uric acid elevation during favipiravir treatment. Favipiravir is metabolized to an inactive metabolite M1 by aldehyde oxidase and xanthine oxidase, and excreted into urine. In the kidney, uric acid handling is regulated by the balance of reabsorption and tubular secretion in the proximal tubules. Favipiravir and M1 act as moderate inhibitors of organic anion transporter 1 and 3 (OAT1 and OAT3), which are involved in uric acid excretion in the kidney. In addition, M1 enhances uric acid reuptake via urate transporter 1 (URAT1) in the renal proximal tubules. Thus, favipiravir is thought to decrease uric acid excretion into urine, resulting in elevation of uric acid levels in blood. Elevated uric acid levels were returned to normal after discontinuation of favipiravir, and favipiravir is not used for long periods of time for the treatment of viral infection. Thus, the effect on blood uric acid levels was subclinical in most studies. Nevertheless, the adverse effect of favipiravir might be clinically important in patients with a history of gout, hyperuricemia, kidney function impairment (in which blood concentration of M1 increases), and where there is concomitant use of other drugs affecting blood uric acid elevation.A 72-year-old male was diagnosed pneumococcal meningitis and we started treatment with antibacterial drugs and corticosteroids. On the 6th day, his consciousness level decreased. On the 7th day DWI of MRI showed a new infarction in bilateral cerebellar, and MRA showed multiple arterial stenosis. On the 12th day, CT angiography showed expansion of cerebral infarction and progress of diffuse stenosis. After that the stenosis improved over time, it disappeared on the 39th day. These results suggest that vasospasm is involved in the pathology of vascular stenosis.A 66-year-old woman who had myasthenia gravis (MG) admitted for type II respiratory failure and right heart failure. Although she had neither ptosis, eye movement disorder, nor diplopia, she had orbital muscles weakness, reduction of gag reflex, dysarthria, dysphagia, and mild proximal muscle weakness. Blood tests showed anti-striated muscle antibodies (anti-titin antibody and anti-Kv1.4 antibody). A muscle biopsy of the left biceps showed a marked variation in fiber size, mild mononuclear cell infiltration was seen surrounding blood vessels in perimysium and nemaline bodies in some fibers. Immunohistochemical stains showed many muscle fibers express HLA-ABC. The patient was diagnosed as sporadic late-onset nemaline myopathy (SLONM) with MG, and treated by tacrolimus. After treatment, her respiratory function gradually improved and she discharged. In the case of atypical MG, measurement of anti-striated muscle antibody or muscle biopsy should be considered.A 79-year-old man presented with chest and back pain on the right side but with no cutaneous lesions. He had received oral corticosteroids and immunosuppressants for systemic lupus erythematosus. He had spastic paraplegia, sensory disturbance in the lower limbs, and dysfunction of the bladder and bowel. He showed mononuclear-dominant pleocytosis and elevated proteins in the cerebrospinal fluid (CSF), and a decreased CSF/blood glucose ratio. Although polymerase chain reaction techniques found no varicella-zoster virus (VZV) DNA, VZV IgG antibodies were elevated in both the serum and CSF, and the VZV IgG index was dramatically elevated. MRI revealed no lesions in the brain or spine. However, somatosensory evoked potentials in the tibial nerve showed abnormal prolongation of the central sensory conduction time. We diagnosed the patient with acute myelitis associated with zoster sine herpete (ZSH). He received acyclovir and intravenous methylprednisolone pulse therapy in the early stage, and his symptoms and CSF findings completely recovered. We conclude that acute myelitis associated with ZSH should be treated as soon as possible because VZV infection may induce necrotizing myelitis if the treatment is delayed.This is the rare case report that bilateral vagus nerve paralysis was emerged as the initial symptom of acute myelogenous leukemia (AML). An 83-year-old man admitted to our hospital because of dysphagia. His dysphagia progressed two months prior to admission. Although physical examination revealed no abnormality, videoendoscopy and videofluorography examination clearly revealed bilateral vagus nerve palsy. Brain MRI showed hypointense signals at the bilateral clivus on T1 weighted images, suggesting tumor infiltration to bilateral petroclivus. He was diagnosed as AML by blood samples and bone marrow biopsy. After initiation of the treatment including radiation therapy, dysphagia shows mild improvement. https://www.selleckchem.com/products/nd-630.html Although bilateral cranial nerve palsy due to malignant tumor involving at the clivus is very uncommon, we should pay attention to the symptom.A 48-year-old woman with a right-sided headache beginning a month prior to admission presented with sudden-onset right hemiparesis. On admission, she had weakness of the right lower extremity, which disappeared 3 hours after onset. Contrast enhanced brain MRI revealed no parenchymal lesion, while indicated thrombi in the superior sagittal sinus and the right side of the transverse sinus, sigmoid sinus, and internal jugular vein, leading to the diagnosis of cerebral venous sinus thrombosis. Brain perfusion single photon emission computed tomography presented slightly decreased blood flow in the bilateral frontal lobes (left-sided dominant) and the right occipitotemporal lobe. Electroencephalogram showed no abnormal finding. After anticoagulant therapy, thrombi in the venous sinuses decreased and brain blood flow improved. We should consider cerebral venous sinus thrombosis in the case of a patient presenting with symptoms of a transient ischemic attack accompanied with headache. Moreover, the etiology of transient neurological deficits remains controversial.